Yi Sun

Intraplacental choriocarcinoma coexisting with fetomaternal hemorrhage and fetal intrahepatic portosystemic venous shunt in a term pregnancy: A case report

Rationale: Intraplacental choriocarcinoma (IC) coexisting with fetomaternal hemorrhage (FMH) in term pregnancy is rare and life-threatening for the mother and baby. The limited knowledge of this disease leads to delayed or missed diagnosis. This case report aims to illustrate how to avoid missed diagnosis through a more complicated case by the presence of fetal intrahepatic portosystemic venous shunt (IPSVS). Patient concerns: A 39-week pregnant woman presented to our hospital with decreased fetal movements. Diagnoses: Prenatally, the ultrasound examination identified the presence of IPSVS. FMH was diagnosed immediately after delivery, and the diagnosis was subsequently revised to IC with FMH 41 days postpartum when the mother developed symptoms of vaginal bleeding. Interventions: The mother received chemotherapy. Surveillance was conducted through measurements of beta human chorionic gonadotropin (β-hCG) and computed tomography imaging. The infant underwent β-hCG testing and ultrasound examinations for IPSVS. Outcomes: Following 6 cycles of chemotherapy, the mother’s β-hCG levels normalized, with complete resolution of pulmonary metastases. The infant’s β-hCG test results were negative, and no significant change was observed in the IPSVS. Lessons: IC coexisting with FMH is rare. Enhancing the understanding of the manifestations of this disease is vital for its early diagnosis. When unexplained FMH occurs, a systematic investigation into potential etiologies is necessary, and clinicians should remain vigilant for the possibility of IC. This case underscores the importance of thorough placental pathological examination and postpartum HCG monitoring for patients with FMH.

The TRIM22-CDT2 axis is the key mediator of the p53-Rb signals in growth control of HPV-positive cervical carcinoma cells

Persistent infection with high-risk human papillomavirus (HPV) is the primary contributor to the development of cervical cancer. Although HPV oncoproteins E6 and E7 clearly trigger cervical tumorigenesis by inactivating p53 and Rb pathways, the downstream mediators of p53/Rb inactivation remain elusive. Here we report that CDT2, a subunit of Cullin-RING ligase 4 (CRL4), is significantly upregulated in cervical carcinoma tissues, which correlates with E6/E7 expression and poor patient survival. Mechanistically, E7-mediated Rb degradation upregulates E2F1, which in turn increases CDT2 transcription, whereas E6-mediated p53 degradation downregulates TRIM22, a novel E3 ligase for CDT2 degradation, leading to CDT2 accumulation to promote growth and survival of cervical cancer cells. Importantly, CDT2 depletion induces DNA aneuploidy and senescence via stabilization of histone lysine methyltransferase SET8, a CRL4